[PATH] Bones, Joints and Soft Tissue (Part 1 BONE) [Martin] Flashcards
This image depicts what type of process?
Endochondral ossification
(in a calcaneus)
Root word association:
Osteoporosis =
Osteomalacia =
Osteopetrosis =
Osteogenesis imperfecta =
Osteitis deformans =
Osteodystrophy =
Osteoporosis = Porous; thinned out bone
Osteomalacia = Weakened, soft bone
Osteopetrosis = Peter=rock, stone bone
Osteogenesis imperfecta = Imperfect origin of bone
Osteitis deformans = Deforming bone-itis
Osteodystrophy = Difficult/bad growing bone
What are the (2) components of bone matrix?
Osteoid
Mineral component
Hardness of bones is due to?
Hydroxyapatite
What are the components of osteoid?
Type I collagen with small amounts of glycosaminoglycans and other proteins
What is the protein found in osteoid?
Produced by what?
Function?
How can you utilize osteopontin levels?
Osteopontin (aka osteocalcin)
- produced by osteoblasts
- function: contributes to the regulation of bone formation, mineralization, and calcium homeostasis
- utilization: serum osteopontin levels are used as a sensitive and specific marker of osteoblast activity
What are the (2) histologic forms of bone?
Woven
Lamellar
Characteristics of woven bone?
- Disorganized
- Haphazard arrangement of collagen= less structural integrity
- Produced rapidly ; fetal development and fracture repair
- Abnormal in adults, but not specific for any bone disease
Characteristics of lamellar bone?
Slow production
Parallel collagen
Strong
Function of osteoblasts
Synthesize, transport and assemble matrix
*Regulates mineralization
Function of osteocytes?
-Inactive osteoblasts (inactive osteoblasts can be recognized by a decrease in cytoplasmic volume)
- Control calcium and phosphate levels
- detect mechanical forces and translate them into biological activity in a process known as mechanotransduction
How are osteocytes interconnected?
by an intricate network of dendritic cytoplasmic processes through tunnels (canaliculi)
What are osteoclasts?
Function?
Multinucleated macrophages derived from circulating monocytes
Bone resorption
What is a resorption pit?
When surface integrin proteins allow osteoclasts to attach to the matrix and create a sealed extracellular trench (a resorption pit)
-Secretion of acid and neutral proteases, predominantly matrix metalloproteases (MMPs), into the pit results in dissolution of inorganic and organic components of bone
What type of bone is associated with:
Endochondral ossification?
Intramembranous ossification?
Endochondral ossification = Long bones
Intramembranous ossification = Flat bones
What is the name for the cartilage mold that bones develop from during endochondral ossification?
anlagen
A central medullary canal within the anlagen is created by what in the process of endochondral ossification?
chondroblasts
In the process of endochondral ossification, where do osteoblasts begin to deposit the cortex?
beneath the periosteum of the diaphysis (midshaft)
-this forms a primary center of ossification resulting in radial growth
During endochondral ossification, where is new bone deposited?
- new bone is deposited at the bottom of growth plates (epiphyses)
- this leads to longitudinal growth (secondary centers of ossification)
What is the general process of intramembranous ossification? What type of growth is involved in this process?
- mesenchyme is directly ossified by osteoblasts, there is no cartilage anlagen
- Appositional growth: direct deposit of new bone on pre-existing surface
What are the different zones seen in an active growth plate with ongoing endochondral ossification?
reserve zone, proliferation, hypertrophy, mineralization, and primary spongiosa
Where does remodeling of bone take place? What does it consist of? What is it regulated by?
- within the bone (or basic) multicellular unit (BMU)
- consists of a unit of coupled osteoblast and osteoclast activity on the bone surface
- regulated by cell-cell interactions and cytokines
When is peak bone mass achieved?
Early adulthood after cessation of skeletal growth
At what point is bone resorption > formation?
-fourth decade
RANK
What is it?
Where is it expressed?
Function?
What is it: receptor activator for NF-kB
Where is it expressed = Osteoclast precursors
Function = Breakdown; when stimulated by RANKL, activates transcription factor NF-kB, which is essential for generation and survival of osteoclasts
RANK-L
Where is it expressed?
Function?
Where is it expressed = Osteoblasts and marrow stromal cells
Function = Breakdown
OPG
Where is it expressed?
Function?
Where is it expressed = “Decoy” receptor made by osteoblasts that can bind RANKL and prevent it’s interaction with RANK
Function = Build
What is the function of WNT/B-catenin?
WNT proteins (produced by osteoprogenitor cells) bind to LRP5 and LRP6 receptors on osteoblasts → thus trigger activation of B-catenin and production of OPG
A product produced by osteocyte inhibits the WNT/Beta-catenin pathway. What is it? What happens if the WNT/B-catenin pathway is blocked?
- Sclerostin
- if it is blocked then it suppresses bone formation
The balance between net bone formation and resorption is modulated by what two things?
-RANK
&
-WNT
What are the common building circulating hormones/factors?
Estrogen
Testosterone
Vit D
What are the common breakdown circulating hormones/factors?
PTH
IL-1
Glucocorticoids
What is M-CSF?
Macrophage colony stimulating factor
Function of M-CSF?
M-CSF receptor on osteoclast precursors STIMULATES tyrosine kinase cascade that is crucial for generation of osteoclasts
What type of cell signaling occurs between osteoclasts and osteoblasts? What occurs during this cell signaling?
- Paracrine crosstalk between osteoblasts and osteoclasts
- breakdown of matrix by osteoclasts liberates and activates matrix proteins, growth factors, cytokines, and enzymes; some of which stimulate osteoblasts
- breakdown of bone to its elemental units which are released into the microenvironment stimulate its renewal
What are the (3) primary developmental disorders of bone?
Osteogenesis imperfecta
Osteopetrosis
Mucopolysaccharidoses
What is dysostosis and what is commonly associated with this?
- localized disruption of migration and condensation of mesenchyme and differentiation into cartilage anlage
- Transcription factor defects: specifically homeobox genes
What happens if there is a defect in homeobox proteins?
abnormal differentiation in osteoblasts and chondrocytes
Which gene is associated with Brachydactyly types D and E?
What is the disease manifestation?
HOXD13
-short terminal phalanges of thumb and big toe
Which gene mutation is associated with cleidocranial dysplasia?
RUNX2
What are the disease manifestations of cleidocranial dysplasia?
Inheritance pattern:
Presentation: six things
Inheritance pattern: AD
Presentation:
- patent frontanelles
- delayed closure of cranial sutures
- Wormian bones
- Delayed eruption of secondary teeth
- Primitive clavicles
- short height
Define:
Dysplasia
Global disorganization of bone &/or cartilage
Define:
Syndactyly/Craniosynostosis
Abnormal fusion of bones
What are wormian bones?
Extra bones within cranial sutures
What is an excellent way to determine the origin of a dwarfism pathology?
Can you give examples?
Look at the chest cavity!
Normal trunk length with achondroplasia
Small chest cavity with thanatophoric dysplasia
Achondroplasia
Gene mutation?
Presentation?
Mortality?
Gene mutation = Autosomal dominant FGFR3 gain of function
Presentation = Short extremities, normal trunk length, enlarged head, bluging forehead, depression root of nose
Mortality = NO change in longevity, intelligence or reproductive status
Thanatophoric dysplasia
Gene mutation?
Pathophysiology?
Presentation?
Mortality?
Gene mutation = FGFR3 gain of function (more severe phenotype)
Pathophysiology= diminished proliferation of chondrocytes and disorganization in the zone of proliferation
Presentation = Small chest cavity, bell-shaped abdomen, micromelic shortening of limbs, frontal bossing
Mortality = Die at birth or soon after
What is another name for osteogenesis imperfecta and what type of disease is this?
- aka Brittle bone disease
- deficiencies in type I collagen synthesis; most common inherited disorder of connective tissue
What causes osteogenesis imperfecta (OI)?
it is caused by mutations in genes encoding the alpha1 and alpha2 chains of type 1 collagen → mutated collagen peptides and no triple helix formation
Osteogenesis imperfecta:
Which type has the best prognosis?
Worst?
Best = Type I
Worst = Type 2
- mutant collagen is associated with severe or lethal forms
- decreased synthesis of normal collagen = mild skeletal abnormalities
What are the features of Type II OI?
- there is no triple helix, it is uniformly fatal in utero, there is extraordinary bone fragility with multiple intrauterine fractures
- the collagen is improperly formed
What are the features of Type I OI?
- normal life span, childhood fractures that decrease in frequency following puberty
- the collagen structure is normal, but the amount is < normal
Prognosis of Type II osteogenesis imperfecta?
Uniformly fatal in utero
Buzz word association for osteogenesis imperfecta type 2?
“Accordion-like” shortening of the limbs
What is the collagen defect associated with type I OI?
COL1A1
What is the collagen defect associated with Type II OI?
COL1A1 or COL1A2
What is the most severe subtype of OI in babies who do not die as newborns?
type III
What are the major clinical features of osteogenesis imperfecta?
Blue sclera
Skeletal fragility
Dentinogenesis imperfecta (small teeth)
Hearing impairment
Joint laxity
What is the most common type of osteogenesis imperfecta?
Type I
Also the mildest type of OI
Why is type II typically fatal?
Respiratory problems
(They have underdeveloped lungs from small thoracic cage)
What is the difference in sclera appearance b/w Type III and Type IV OI?
Type III = Blue, purple or gray tint
Type IV= White
*Remember; The order of best prognosis to worst is (1–> 4 –>3–>2) because fuck, lets make this difficult. But yeah, remember that type 4 is less severe, so the sclera are going to be normal in color.
What is the treatment of OI?
- surgical rodding of long bones
- exercise, keep a healthy weight, good nutrition
- don’t smoke, don’t take steroids
What types of fractures are typically observed in both child abuse and OI?
- fractures in multiple stages of healing
- rib fractures
- spiral fractures
- fractures for which there is no adequate explanation of trauma
What is the best way to tell the difference between OI and child abuse?
bone pathology
Osteopetrosis
Aka?
Marble bone disease
What is the pathophysiology of osteopetrosis aka marble bone disease?
decreased bone resorption due to deficient osteoclast development/function → diffuse, symmetric skeletal sclerosis
What is Albers-Schonberg disease?
gene mutation?
What does it code for?
a mild autosomal dominant form of osteopetrosis
- gene mutation= CLCN7
- encodes a proton-chloride exchanger on the osteoclast surface that is required for resorption pit acidification
What is the cause of most cases of autosomal recessive osteopetrosis?
What does this encode?
a mutation of TCIRG1
-encodes a subunit of the osteoclast vacuolar H+-ATPase that is also necessary for acidification of the resorption pit
What is the deficiency in other causes of autosomal recessive osteopetrosis?
Carbonic anhydrase 2 (CA2)
What is the function of carbonic anhydrase 2 (CA2)?
-What is often associated with deficiency of CA2?
it is required by osteoclast and renal tubular cells to generate protons from carbon dioxide and water
-renal tubular acidosis
What are the features of osteopetrosis?
bones lack a medullary cavity, bulbous ends of long bones, neural foramina are small and compress nerves
-deposited bone is not remodeled and tends to be woven rather than lamellar
How does osteopetrosis appear on Xray?
Buzz word association?
Erlenmeyer flask
Inheritance pattern for osteopetrosis-severe infantile type?
Populations?
Autosomal recessive
Mediterranean and Arab race
Common clinical features of osteopetrosis- severe infantile type?
- Postpartum mortality: fractures, anemia, and hydrocephaly; repeated (fatal) infection due to leukopenia
- extramedullary hematopoiesis leads to hepatosplenomegaly
Cranial nerve deficits:
Optic atrophy, deafness, facial paralysis
What are the features of the autosomal dominant form of osteopetrosis?
- mild
- diagnosed in adolescence or adulthood
How can osteopetrosis be treated?
hematopoietic stem cell transplantation
What is seen on histology with osteopetrosis?
No medullary cavity
What type of disease is mucopolysaccharidoses?
Lysosomal storage disease
What is mucopolysaccharidoses?
- What enzymes are mostly affected?
- Where do mucopolysaccharides accumulate?
- deficiency in enzymes that degrade dermatan sulfate, heparan sulfate, and keratan sulfate
- Mostly acid hydrolase enzymes affected
- mucopolysaccharides accumulate in the chondrocytes
What is the result of extracellular mucopolysaccharide accumulation?
structural defects in articular cartilage
what are the clinical manifestations of mucopolysaccharidoses?
short stature, chest wall abnormalities, and malformed bones
What are examples of acquired bone disorders (5)?
Osteopenia/osteoporosis
Pagets
Osteomalacia/rickets
Hyperparathyroidism
Renal osteodystrophy
What are 3 primary causes of osteoporosis?
- idiopathic
- postmenopausal
- senile
Define osteopenia
Define osteoporosis
Osteopenia = decreased bone mass: 1.0 - 2.5 standard deviations below the mean
Osteoporosis = Osteopenia severe enough to increase risk of fracture. Bone mass at least 2.5 SD below the mean peak bone mass in young adults
If your patient has a bone mass that is less than 2.5 SD below the mean, but you still diagnose them with osteoporosis, what MUST have happened? aka what signifies osteoporosis?
Atraumatic
or
Vertebral compression fractures
What are the most common forms of osteoporosis?
senile and postmenopausal
the magnitude of deficits in bone formation that accrues with every resorption and formation cycle is determined largely through what?
magnitude determined largely through hereditary factors
Normal age-related bone loss average is what?
- 7% per year
- equal loss between sexes
- more rapid in caucasians than those of African descent
How is senile osteoporosis classified?
What are the features of senile osteoporosis?
- senile osteoporosis is classified as a low turnover variant
- age-related changes include a reduced proliferative and biosynthetic potential (decreased capacity to make bone)
- decreased cellular response to growth factors
How does physical activity affect the rate of osteoporosis?
decreased physical activity leads to an increased rate of bone loss
-mechanical forces stimulate an increase in normal bone remodeling
When considering physical activity, which exercise is better in the prevention against osteoporosis? Why?
- resistance exercises are better
- the effect of load magnitude on bone density is greater than load repetition
What genetic factors could contribute to osteoporosis?
- LRP5 single gene defect (rare)
- polymorphisms in certain genes may contribute to variation in peak bone density within populations (most common are: RANKL, OPG, RANK, HLA locus, estrogen receptor gene, vit D receptor gene)
What population is at risk of never obtaining their full potential bone mass due to eating disorders?
Adolescent girls
(Insufficienct calcium intake during period of rapid growth restricts their peak bone mass)
How do calcium, PTH, and vitamin D contribute to the pathogenesis of senile osteoporosis?
calcium deficiency, increased PTH, and decreased vitamin D all contribute to senile osteoporosis
What is a major hormonal influence on osteoporosis?
Menopause
(estrogen deficiency)
How does decreased estrogen lead to osteoporosis and what variant is estrogen deficiency classified as?
decreased estrogen leads to an increase in both resorption and formation, but formation < resorption
- high turnover variant
- decreased estrogen leads to an increase in inflammatory cytokines (IL-6, TNF, and IL-1) → increased RANKL and decreased OPG → increased osteoclast recruitment and activity
Chemotherapy for what cancer has an association with an increased risk of developing osteoporosis?
standard therapies for breast cancer (Tamoxifen) can increase bone loss
What is the histological hallmark of osteoporosis?
normal bone, decreased in quantity
Which types of bones are likely to be affected by postmenopausal osteoporosis?
How does postmenopausal osteoporosis affect these bones?
- bones with increased surface area (cancellous bones of vertebral bodies)
- the trabecular plates become perforated and thinned and lose their interconnections leading to microfractures and vertebral collapse
How does senile osteoporosis affect bones?
the cortex becomes thinned by subperiosteal and endosteal resorption, and the Haversian systems are widened
Describe the appearance of osteoporotic bone
(Right)
Loss of horizontal trabeculae and thickened vertical trabeculae
What is the clinical course of osteoporosis?
- vertebral fractures: thoracic and lumbar
- loss of height
- fractures of femoral neck, pelvis, or spine → immobilization
What spinal changes are associated with loss of height in osteoporosis?
Lumbar lordosis & kyphoscoliosis
What are 3 methods of prevention used against osteoporosis?
exercise, calcium, and vitamin D
What are 4 methods of treatment for osteoporosis?
- bisphosphonates (decrease osteoclast activity and induce apoptosis)
- hormone therapy
- Denosumab (anti-RANKL) (tx for postmenopausal osteo)
- Anti-sclerostin and Cathepsin K inhibitors (investigational)
What is the method of diagnosis for osteoporosis?
DEXA-scan
-early signs may not even show up on an x-ray (need more than 30% bone loss to detect on plain film)
Why are blood tests used when diagnosing osteoporosis?
to check for secondary causes of osteoporosis, such as renal or hepatic failure, hyperthyroidism
Risk factors for osteoporosis?
Caucasian, light colored eyes and skin
Nutrition (too much phosphorus-soda)
Smokers
What do rickets and osteomalacia have in common in regards to their pathogenesis?
both are manifestations of vitamin D deficiency or its abnormal metabolism
-there is impairment of mineralization leading to accumulation of unmineralized matrix
What is the main difference between osteoporosis and rickets/osteomalacia?
- with osteoporosis the mineralization of bone is normal, the bone mass is just decreased
- with rickets/osteomalacia, there is an impairment of mineralization and resultant accumulation of unmineralized matrix
What is rickets?
rickets refers to the disorder in children, in whom it interferes with the deposition of bone in the growth plates
What is osteomalacia?
the adult counterpart, in which bone formed during remodeling is undermineralized and predisposed to fractures
What are 4 other causes of rickets?
renal rickets, hypophosphatemia, malabsorption, short-gut syndrome
What is the clinical manifestation of rickets?
frontal bossing
squared off head
rachitic rosary of ribs
anterior protrusion of chest, pigeon breast deformity
lumbar lordosis
bowed legs
What is the function of PTH?
calcium homeostasis →net result of PTH = increased serum calcium
What effect does PTH have on calcium homeostasis? (4 things)
- osteoclast activation (increased bone resorption and Ca2+ mobilization. PTH mediates the effect indirectly by increasing RANKL expression on osteoblasts)
- increased resorption of Ca2+ by renal tubules
- increased urinary excretion of phosphates
- increased synthesis of active vitamin D by the kidneys
What are the two types of hyperparathyroidism and what are their causes?
- primary: autonomous parathyroid secretion
- secondary: underlying renal disease (usually less severe than primary)
Elevated PTH is responsible for bone changes in primary hyperparathyroidism, but additional factors contribute in secondary hyperparathyroidism. What are these factors?
chronic renal insufficiency
hyperphosphatemia
metabolic acidosis and aluminum deposition
Hyperparathyroidism leads to significant skeletal changes related to _____ _______ _______
-this leads to what?
unabated osteoclast activity
-leading to increased bone fractures, bone deformities, and joint problems
What are the 3 skeletal abnormalities seen with untreated primary hyperparathyroidism?
- osteoporosis
- brown tumors
- osteitis fibrosa cystica
How does osteoporosis present in cases of hyperparathyroidism?
- most severe in the phalanges, vertebrae, and proximal femur
- there is increased osteoclast activity most prominent in cortical bone, medullary bone not spared
What is dissection osteitis?
What disease is it associated with?
- when clasts tunnel into and dissect centrally along the length of trabeculae, adjacent marrow spaces are replaced by fibrovascular tissue
- gives the appearance of railroad tracks
- associated with hyperparathyroidism
What is the histology associated with hyperparathyroidism?
Train tracks
what is a brown tumor?
bone loss predisposes to microfractures, secondary hemorrhage, macrophage recruitment, and ingrowth of reparative fibrous tissue → mass lesion
what makes brown tumors brown?
vascular, hemorrhage, and hemosiderin deposition; can undergo cystic degeneration
What is von Recklinghausen disease of bone?
What disease is it associated with?
- the combination of increased bone cell activity, peritrabecular fibrosis, and cystic brown tumors
- hallmark of severe hyperparathyroidism
- aka generalized osteitis fibrosis cystica
What is renal osteodystrophy?
-skeletal changes that occur in chronic renal disease, including those associated with dialysis
what are 3 different histologic bone changes associated with renal osteodystrophy?
- high-turnover osteodystrophy: increased bone resorption and bone formation; resorption > formation
- low-turnover or aplastic disease: adynamic bone (little osteoclastic and blastic activity) and less commonly osteomalacia
- mixed pattern of disease: areas with high turnover and low turnover
Kidney disease causes skeletal abnormalities through 3 mechanisms- what are these mechanisms?
- tubular dysfunction
- secondary hyperparathyroidism
- decreased biosynthetic function: decreased vitamin D hydroxylation
What is occurring in tubular dysfunction that leads to renal osteodystrophy?
renal tubular acidosis, associated systemic acidosis dissolves hydroxyapatite → matrix demineralization and osteomalacia
what is occurring in secondary hyperparathyroidism to lead to renal osteodystrophy?
there is a decrease in phosphate excretion, chronic hyperphosphatemia, and hypocalcemia
Which population is renal osteodystrophy most serious?
children- because their bones are still growing
What are 2 consequences of renal osteodystrophy occurring in children?
- renal rickets: when the legs bend inward or outward
- short stature
Paget disease aka?
What is occurring in this disease?
Osteitis deformans
-increased but disordered and structurally unsound bone mass
Paget disease
Characteristsics?
Gene?
Polyostotic (involves multiple bones) (85% of cases)
70yo average age
Caucasians
SQSTM1 gene
What is the pathogenesis of Paget Disease?
uncertain, but both genetic and environmental contributions
50% familial and 10% of sporadic cases are associated with mutations in the SQSTM1 gene
what happens when the SQSTM1 gene is mutated?
there is increased activity of NF-kB leading to increased osteoclast activity
Paget disease
Buzz word association with Xray appearance?
“Cotton Wool”
What is the paget disease hallmark morphology?
Mosaic pattern of lamellar bone seen in sclerotic phase
Jigsaw-like appearance with prominent cement lines
what are the 3 stages of Paget?
- initial osteolytic stage
- mixed osteoclastic-osteoblastic phase
- burned-out quiescent osteosclerotic stage
what are the characteristic features associated with the initial osteolytic stage?
large osteoclasts with 100 nuclei
what are the characteristic features associated with mixed osteoclastic-osteoblastic phase?
clasts persist, but lots of blasts also; primarily osteoblastic at end of stage
what are the characteristic features associated with burned-out quiescent osteosclerotic stage?
osteoblast activity predominates
-coarsely thickened trabeculae and cortices that are soft and porous, lacking structural stability; fractures easily
What is the most dreaded complication of Paget disease?
sarcomatous transformation
-seen in less than 1% of cases, often osteosarcoma or fibrosarcoma in long bones, pelvis, skull, and spine
What type of fractures are associated with paget disease?
-Chalk stick type fractures in the long bones of legs
-Compression fractures of spine → spinal cord injury and kyphosis
What are the lab values associated with paget disease?
Elevated serum ALK PHOSPHATASE
NORMAL = Calcium and phosphorous
Name a unique clinical feature of paget disease
Hypervascularity of paget disease
Warms the overlying skin
→ Can lead to high output heart failure
What is the treatment for Paget disease?
calcitonin and bisphosphonates to suppress symptoms
Define:
Simple fracture
Overlying skin intact
Define:
Compound fracture
Bone communicates with the skin surface
Define:
Comminuted fracture
Bone is fragmented
Define:
Displaced fracture
Ends of the bone at the fracture site are not aligned
Define:
Stress fracture
Slowly developing fracture that follows a period of increased physical activity in which bone is subjected to repetitive loads
nice.
Define:
Greenstick fracture
Extending only partially through the bone, common in infants when bones are soft
Define:
Pathologic fracture
Involving bone weakened by an underlying disease process such as a tumor
What is osteonecrosis?
Infarction of the bone and marrow
(pretty common)
What causes most cases of osteonecrosis?
Fractures
or
Corticosteroid tx (iatrogenic)
How do subchondral infarcts present?
What is the morphology of subchondral infarcts?
they cause pain initially associated only with activity then becomes constant
- subchondral infarcts often collapse and may lead to severe secondary osteoarthritis
- they are triangular or wedge-shaped with the subchondral bone plate as its base → necrosis
How do medullary infarcts typically present?
they are usually small and clinically silent
What region is typically not affected in osteonecrosis?
Why?
Cortex is not affected
Due to collateral flow
Buzz word association with osteonecrosis?
“Creeping substitution”
What is osteomyelitis?
Inflammation of the bone and marrow
Typically following infection
What are most cases of osteomyelitis caused by?
Pyogenic bacteria
&
Mycobacteria
How does pyogenic osteomyelitis typically spread in:
Kids?
Adults?
Kids = Hematogenous
Adults = Complication of open fractures, surgical procedures and diabetic infections
Most common cause of pyogenic osteomyelitis?
Staph aureus (80-90%)
Osteomyelitis:
Name the associated organism with:
Sickle cell patients
Salmonella
Osteomyelitis:
Name the associated organism with:
MAC deficiency
Neisseria
What is:
Sequestrum?
Involucrum?
Sequestrum = Dead bone following abscess
Involucrum = New bone
What is the histology associated with mycobacterial osteomyelitis?
Caseous necrosis and granulomas
What is Pott disease?
Aka Tuberculous spondylitis
Permanent compression fractures
What are the associated bone deformities seen with skeletal syphilis?
Saber shin
Saddle nose
what are the characteristic features associated with burned-out quiescent osteosclerotic stage?
osteoblast activity predominates
-coarsely thickened trabeculae and cortices that are soft and porous, lacking structural stability; fractures easily
